The aim is to refine and develop the consequences of a mathematical model for transcriptional control of proliferation. The model exhibits a critical instability which depends on propagated variability of kinetic parameters or of equational distribution of the critical macromolecules, and it predicts heterogeneity of proliferative potential and cycle times in a growing population. The model predicts death of subcritical cells, and may be applicable to the analysis of ageing and to death during organogenesis. Relating subcritical death involves an analysis of the concept of coordination among linked parallel reaction sequences. The refinement of the model requires introduction of a greater number of variables; and the mathematical problems raised by this will be dealt with by simulation. The origin of possible propagated variability will be explored by tracing the influence of elementary random events on the development of the biosynthetic system through successive proliferative cycles. Application of the approach to differentiation will involve study of known models (Britten-Davidson, Georgiev) of transcriptional control as dynamic systems, in order to ascertain what classes of stimuli to specific differentiation, if any, will induce bifurcation in such models. As a model of aging, our system suggests possible avenues of constructive interference with the aging process at the molecular level. For atherogenesis, the model not only offers general illumination of the natural history of the disease, but suggests a possible specific link to cholesterol esters, known to be inciting factors, by way of the role of cholesterol esters in the activation of key transcriptional and translational enzymes.